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a significant protein-protein interaction between GR and CHOP (show DDIT3 Proteins), (GR-CHOP (show DDIT3 Proteins) heterocomplex formation) under endoplasmic reticulum stress conditions, is reported.
This study identifies an endocrine developmental axis in which fetal GR primes the activity of PPARalpha (show PPARA Proteins) in anticipation of the sudden shifts in postnatal nutrient source and metabolic demands.
Skin differentiation is impaired, and both apoptosis and cell proliferation are augmented in the absence of p23 (show CDK5R1 Proteins); the consequences are a severe thinning of the stratum corneum and reduced numbers of hair follicles. Since the phenotype of p23 (show CDK5R1 Proteins)-null embryos is strikingly similar to that of embryos lacking the glucocorticoid receptor, a paradigmatic Hsp90 (show HSP90 Proteins)-p23 (show CDK5R1 Proteins) client protein, we investigated glucocorticoid signaling.
REV-ERBalpha (show NR1D1 Proteins) binds to the C-terminal portion and GR to the N-terminal portion of HSP90alpha (show HSP90AA2 Proteins) and HSP90beta (show HSP90AB1 Proteins), a chaperone responsible for the activation of proteins to ensure survival of a cell.
Phospho-AMPK (show PRKAA1 Proteins) is a molecular switch able to cooperate with glucocorticoid receptors and Ppar-alpha (show PPARA Proteins) at the chromatin level, a novel adaptation mechanism to prolonged fasting.
GR signaling decreases NRF2 (show NFE2L2 Proteins) transcriptional activation through reducing the NRF2 (show NFE2L2 Proteins)-dependent histone acetylation. Consistent with these observations, GR signaling blocked NRF2 (show NFE2L2 Proteins)-mediated cytoprotection from oxidative stress.
GRbeta antagonizes the GC-induced signaling during fasting via GRalpha and the PPARalpha (show PPARA Proteins)-FGF21 (show FGF21 Proteins) axis that reduces fat burning. Furthermore, hepatic GRbeta increases inflammation, which leads to hepatic lipid accumulation.
liver-specific deletion of GR resulted in a significant increase in mRNA expression of key genes involved in gluconeogenesis and glycogen (show GYS1 Proteins) metabolism in kidney tissue, indicating a compensatory mechanism to maintain glucose homeostasis. Liver GRKO mice demonstrated decreased fat mass and liver glycogen (show GYS1 Proteins) content compared with WT mice administered dexamethasone for 2 weeks.
These results established a novel role for GR and KLF13 (show KLF13 Proteins) signaling in adult cardiomyocytes with potential clinical implications for the prevention of cardiotoxicity induced heart failure.
miR (show MLXIP Proteins)-433 helps maintain circadian rhythm in osteoblasts by regulating sensitivity to glucocorticoid receptor signaling.
The guinea pig GR-specific mutations within the H1-H3 loop confer global changes within the GR-Hsp90 (show HSP90 Proteins) complex that favor FKBP51 (show FKBP5 Proteins) repression over FKBP52 (show FKBP4 Proteins) potentiation.
A woman with glucocorticoid resistance and her mother had a novel p.Arg477Cys (c.1429C>T) mutation in exon 4 of NR3C1, in the 2dzinc finger of the DNA-binding domain. Its 'in silico' functional effect was assessed using pathogenicity prediction software, being characterized as pathogenic. An unrelated patient had a novel p.His588Leufs*5 (c.1762_1763insTTAC) mutation, in exon 6, in the ligand binding domain.
NR3C1 as an important gene of the hypothalamic-pituitary-adrenal axis seems to be particularly relevant for the pathophysiology of ADHD combined with comorbid CD.
The impact of AKT1 (show AKT1 Proteins) on glucocorticoid receptor (GR)-induced transcriptional activity in cooperation with phospho-serine/threonine-binding protein 14-3-3 (show YWHAQ Proteins), was examined.
Childhood Maltreatment and MDD are both associated wit haltered DNA methylation (show HELLS Proteins) levels in the NR3C1 promoter region, however the location and direction of effects differ between the two exposure.s
This study presents evidence of reduced methylation of NR3C1 in association with childhood maltreatment and depressive, anxiety and substance-use disorders in adults.
genetic association studies in a racially diverse population in North Carolina: Data suggest that an SNP in NR3C1 (rs6191, G3134T, "glucocorticoid receptor beta") is associated with altered gene expression profile in primary macrophages; minor allele frequency is 74% with a higher prevalence in Caucasian non-Hispanic participants.
Decreased DNA methylation (show HELLS Proteins) of CpG1 of NR3C1 in high-risk infants may allow for increased binding of transcription factors involved in the stress response, repair and regulation of NR3C1. This may ensure healthy growth in high-risk preterm infants over increasing cortisol levels.
haplotype TAAT of GR might be a protective factor against aggressive behavior, while gene-gene interactions between GR rs1800445 and MR (NR3C2) rs2070951 might be a risk factor for aggressive behavior in the Central South Chinese Han population
Glucocorticoid receptor (GR) is recruited to activator protein-1 (AP-1) target genes in a DNA-binding-dependent manner.
These results indicate that myostatin (show MSTN Proteins) mediates maternal low protein diet-induced growth retardation, through epigenetic regulation involving FoxO3 (show FOXO3 Proteins) and glucocorticoid receptor binding to its promoter.
Data indicate that higher hepatic glucocorticoid receptor (GR) expression in EHL piglets attributes mainly to the enhanced transcription of GR promoter 1-9/10 from breed-specific interaction of p53 (show TP53 Proteins) and specificity protein 1 (Sp1 (show SP1 Proteins)).
Tissue specificities, gene expression and induction responsiveness of the porcine NR3C1 gene.
Cloning and dna sequence analysis of the upstream flanking region of the NR3C1 gene in the domestic pig.
Effects of age, weaning and/or social isolation on the expression of genes regulating glucocorticoid response [glucocorticoid receptor).
Glucocorticoid Receptor protein expression in granulosa cells was higher in cysts from animals with spontaneous cystic ovarian disease and adrenocorticotropic hormone-induced cystic ovarian disease than in tertiary follicles from control animals.
Exposure to follicular fluid transiently increased the transcript levels of IL8 (show IL8 Proteins) and PTGS2 (show PTGS2 Proteins), and decreased the expression of SOD2 (show SOD2 Proteins), GPX3 (show GPX3 Proteins), DAB2 (show DAB2 Proteins), and NR3C1. TNF (show TNF Proteins) and IL6 (show IL6 Proteins) levels were also decreased while those of NAMPT (show NAMPT Proteins) were unaffected.
Bayesian image analysis of dexamethasone and shear stress-induced glucocorticoid receptor intracellular movement
investigation of gene expression for GR, 11HSD1, and 11HSD2 (show HSD11B2 Proteins) in granulosa cells and theca interna layers during follicular maturation and atresia: expression of GR was largely unchanged during follicular maturation
The E domain of the trout receptors are not involved in the nucleocytoplasmic localization of naive trout GRs (show GARS Proteins), but the A/B domain, especially if linked to the corresponding trout CD region, plays a pivotal role in the cellular distribution pattern.
This gene encodes glucocorticoid receptor, which can function both as a transcription factor that binds to glucocorticoid response elements in the promoters of glucocorticoid responsive genes to activate their transcription, and as a regulator of other transcription factors. This receptor is typically found in the cytoplasm, but upon ligand binding, is transported into the nucleus. It is involved in inflammatory responses, cellular proliferation, and differentiation in target tissues. Mutations in this gene are associated with generalized glucocorticoid resistance. Alternative splicing of this gene results in transcript variants encoding either the same or different isoforms. Additional isoforms resulting from the use of alternate in-frame translation initiation sites have also been described, and shown to be functional, displaying diverse cytoplasm-to-nucleus trafficking patterns and distinct transcriptional activities (PMID:15866175).
, nuclear receptor subfamily 3, group C, member 1
, glucocorticoid receptor 1
, nuclear receptor subfamily 3 group C member 1
, glucocorticoid nuclear receptor variant 1
, glucocorticoid receptor alpha
, glucocorticoid receptor variant P
, glucocorticoid receptor variant beta
, glucocorticoid receptor variant gamma